Zearalenone (ZEA) an estrogenic mycotoxin and, therefore the reproductive system as one of its main targets of toxicity. Besides being a mycotoxin and toxigenic immunosuppressive, the ZEA hematological changes and promotes an imbalance in the oxidative system, especially in antioxidant enzymes. Thus, lycopene, a carotenoid antioxidant potential is considered one of the most potent free radical scavengers and may be used as an alternative therapy to reduce or prevent the toxic effects of ZEA. Male Swiss mice were pretreated with lycopene (20 mg/kg, p.o.) for 10 consecutive days. On the 11th day was held the acute treatment with ZEA (40 mg/kg, p.o.), and after 48 hours was performed euthanasia of animals. We analyzed reproductive, hematological, histological, inflammatory and oxidative stress markers in blood, testes, epididymis, kidneys and livers. ZEA hematotoxicity caused by increased total leukocytes and hemoglobin and hematocrit increased and decreased the number of lymphocytes as well as erythrocytes and platelets. In regard to reproductive and hormonal parameters changes in testicular histology and decreased testosterone levels and sperm motility and count were observed. The activity of GST (Glutathione-S-transferase), GR (Glutathione reductase) and ALA-D (delta aminolevulinic acid dehydratase) was reduced by the action of ZEA in the testes. The glutathione system was amended by ZEA by decreasing the reduced glutathione (GSH) and increased oxidized glutathione (GSSG) and GSH / GSSG. The analyzed pro-inflammatory parameters were increased by the action of mycotoxin. Pretreatment with lycopene prevented the onset of toxic effects induced by ZEA in virtually all parameters and thus, this antioxidant may be used as an alternative to the prevention of damage by ZEA. / A Zearalenona (ZEA) é uma micotoxina estrogênica tendo, portanto, o sistema reprodutivo como um dos seus principais alvos de toxicidade. Além de ser uma micotoxina toxigênica e imunosupressora, a ZEA altera parâmetros hematológicos e promove um desequilíbrio no sistema oxidativo, especialmente nas enzimas antioxidantes. Assim, o licopeno, um carotenóide com potencial antioxidante, é considerado um dos mais potentes scavengers de radicais livres e pode ser utilizado como alternativa terapêutica a fim de reduzir ou impedir os efeitos tóxicos da ZEA. Camundongos Swiss machos foram pré-tratados com licopeno (20 mg/kg, p.o.) por 10 dias consecutivos. No 11° dia foi realizado o tratamento agudo com a ZEA (40 mg/kg, p.o.), e após 48 horas foi realizada a eutanásia dos animais. Analisamos parâmetros reprodutivos, hematológicos, histológicos, inflamatórios e marcadores de estresse oxidativo em amostras de sangue, testículos, epidídimos, rins e fígado dos animais. A ZEA provocou hematotoxicidade através do aumento de leucócitos totais assim como aumento de hemoglobina e hematócrito e diminuiu o número de hemáceas além de linfócitos e plaquetas. Em relação aos parâmetros reprodutivos e hormonais alterações na histologia testicular e diminuição dos níveis de testosterona e da contagem e motilidade espermática foram obervadas. A atividade das enzimas GST (Glutationa-S-transferase), GR (Glutationa Redutase) e ALA-D (Ácido delta aminolevulínico desidratase) foram reduzidas pela ação da ZEA nos testículos. O sistema glutationa foi alterado pela ZEA através da diminuição da glutationa reduzida (GSH) e aumento da glutationa oxidada (GSSG) e da relação GSH/GSSG. Os parâmetros pró-inflamatórios analisados foram aumentados pela ação da micotoxina. O pré-tratamento com o licopeno preveniu o aparecimento dos efeitos tóxicos induzidos pela ZEA em praticamente todos os parâmetros analisados e assim, este antioxidante pode ser utilizado como uma alternativa na prevenção dos danos causados pela ZEA.

No / Male-mediated developmental toxicity has been of concern for many years. The public became aware of male-mediated developmental toxicity in the early 1990s when it was reported that men working at Sellafield might be causing leukemia in their children. Human and animal studies have contributed to our current understanding of male-mediated effects. Animal studies in the 1980s and 1990s suggested that genetic damage after radiation and chemical exposure might be transmitted to offspring. With the increasing understanding that there is histone retention and modification, protamine incorporation into the chromatin and DNA methylation in mature sperm and that spermatozoal RNA transcripts can play important roles in the epigenetic state of sperm, heritable studies began to be viewed differently. Recent reports using molecular approaches have demonstrated that DNA damage can be transmitted to babies from smoking fathers, and expanded simple tandem repeats minisatellite mutations were found in the germline of fathers who were exposed to radiation from the Chernobyl nuclear power plant disaster. In epidemiological studies, it is possible to clarify whether damage is transmitted to the sons after exposure of the fathers. Paternally transmitted damage to the offspring is now recognized as a complex issue with genetic as well as epigenetic components.